Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
The current standard treatment for heart failure is typically centered on medical treatment using angiotensin converting enzyme (ACE) inhibitors, diuretics, beta-blockade, and digitalis. Cardiac resynchronization therapy (CRT) may also be employed, if a biventricular pacing device is implanted. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering synchronized pacing stimulus to both ventricles. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis et al., entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing.”
In view of the potential severity of heart failure, it is highly desirable to predict or detect the condition and to track its progression so that appropriate therapy can be provided. Many patients suffering heart failure are candidates for pacemakers or ICDs. Accordingly, it is desirable to provide such devices with the capability to automatically detect and track heart failure and, in particular, to detect an imminent heart failure exacerbation. Some aspects of the present invention are directed to this end.
Pulmonary edema is a swelling and/or fluid accumulation in the lungs often caused by heart failure (i.e. the edema represents one of the “congestives” of CHF.) Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs, particularly pulmonary venous pressure. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs (i.e. the alveoli). This can cause severe respiratory problems and, left untreated, can be fatal. Pulmonary edema can also arise due to other factors besides heart failure, such as infections. Pulmonary edema can result in dyspnea, which pertains to difficult/labored breathing or to shortness of breath.
One therapy delivered to address pulmonary edema and dyspnea is to administer diuretics to the patient in an effort to reduce the amount of fluids within the lungs of the patient. For example, diuretics such as furosemide or bumetanide can be administered to the patient to reduce a pulmonary fluid overload. (Diuretics are drugs that increase the flow of urine, thus eliminating water from the body, ultimately reducing thoracic fluid levels.)
It would also be desirable to provide improved techniques for predicting, detecting and tracking pulmonary edema, dyspnea and related pulmonary conditions and aspects of the invention are directed to this end.
It is particularly desirable to provide techniques that need not be calibrated to individual patients. In this regard, at least some predecessor detection techniques use transthoracic impedance values to estimate left atrial pressure (LAP) within the patient, from which heart failure or pulmonary edema is tracked. These techniques typically require that a conversion procedure (for converting impedance values into estimated LAP values) be calibrated to each individual patient. A technique that does not require calibration would be quite advantageous.